The histogenesis of giant cell tumour of bone: a model of interaction between neoplastic cells and osteoclasts

• Zheng, M.H. ^[1] ; Robbins, P. ^[2] ; Xu, J. ^[2] ; Huang, Liping ^[2] ; Wood, D.J. ^[2] ; Papadimitriou, J.M. ^[2]
  1. [1] University of Western Australia

     University of Western Australia

     Australia

     
  2. [2] Division of Tissue Pathology. Western Australia Centre for Pathology and Medical Research. Nedlands. Australia
• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 16, Nº. 1, 2001, págs. 297-307
• Idioma: inglés
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• Resumen

  • Giant cell tumour of bone (GCf) is a benign primary neoplasm of a bone characterised by distinctive clinical, radiological and pathological features. Females are slightly more often affected than males, and the majority of patients present between the ages of 20 and 50. GCf is locally aggressive and produces expansive and lytic lesions, most commonly in the epiphyses of long tubular bones. Histologically, it is composed of oval and spindle mononuclear cells, uniformly distributed amongst which are large multinucleated osteoclast-like giant cells. Although the term "Giant Cell Tumour" (and the erroneous historical term ' osteoclastoma ') may imply that it is the multinucleated giant cells which are responsible for the proliferative capacity of the tumour, there is evidence that the stromal-like cells, the major component of the mononuclear cell population, represent the true neoplastic component of the neoplasm. The diagnosis and management of conventional GCT are often challenging and there is considerable current interest in its pathobiology. The precise histogenesis of GCf and the nature of its varying cellular constituents have remained a matter of some controversy. Factors influencing the clinical course and biological aggression of GCT are also unclear. In this selective review, the c linicopathological characteristics of GCT are summarised and current areas of interest in the study of the neoplasm are presented and discussed. Lastly, a hypothetical model of the mechanism of histogenesis and the biological behaviour of GCf is presented.